Relationship between endothelial function and fibrinolysis in early hypertension.
Abnormalities in fibrinolysis, endothelial function, and glucose and lipid metabolism have been reported in hypertension. This study was conducted to examine the interrelationships between fibrinolytic factors, glucose and lipid metabolism, and endothelial function in hypertension. The effects of administering an angiotensin converting enzyme inhibitor, benazepril, were also examined. Blood levels of the following substances were measured in patients with borderline and mild hypertension (n=50, 51+/-19 years) and in age-matched controls (n=10): total cholesterol, triglycerides, tissue plasminogen activator activity and antigen, and plasminogen activator inhibitor type 1 activity and antigen. Insulin sensitivity was assessed by oral glucose tolerance test, and endothelial function was assessed by evaluating changes in diameter of the brachial artery during reactive hyperemia as observed by ultrasonography. Activities of tissue plasminogen activator and plasminogen activator inhibitor type 1 were both elevated in the hypertensive patients. Stepwise multiple regression analysis showed that plasminogen activator inhibitor type 1 antigen correlated with insulin sensitivity, total cholesterol levels, and triglycerides levels (P<.01). Endothelial function was negatively correlated with tissue plasminogen activator activity and antigen (P<.01). The chronic administration of benazepril (5-10 mg/d) for 20 weeks improved insulin sensitivity, endothelial function (6.6+/-3.4-->9.0+/-2.5%, P<.01), and tissue plasminogen activator activity and antigen. These results indicate that abnormalities in fibrinolysis are associated with endothelial dysfunction as well as disorders of glucose and lipid metabolism in patients with borderline and mild hypertension. The treatment of such patients with benazepril appeared to improve the impairment in fibrinolysis and endothelial dysfunction.
Tomiyama
H
H
The Third Department of Internal Medicine, Teikyo University School of Medicine, Ichihara Hospital, Chiba, Japan. h-tomiya@med.teikyo-u.ac.jp
Kimura
Y
Y
Mitsuhashi
H
H
Kinouchi
T
T
Yoshida
H
H
Kushiro
T
T
Doba
N
N
D000328:Adult; D017311:Amlodipine / Q000627:therapeutic use; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D001552:Benzazepines / Q000627:therapeutic use*; D001794:Blood Pressure / Q000187:drug effects; D001916:Brachial Artery; D002121:Calcium Channel Blockers / Q000627:therapeutic use; D002339:Carotid Arteries / Q000000981:diagnostic imaging; D002784:Cholesterol / Q000097:blood; D004452:Echocardiography; D004730:Endothelium, Vascular / Q000502:physiology / Q000503:physiopathology*; D005260:Female; D005342:Fibrinolysis; D005951:Glucose Tolerance Test; D006487:Hemostasis; D006801:Humans; D006940:Hyperemia; D006973:Hypertension / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000503:physiopathology*; D007328:Insulin / Q000502:physiology; D008297:Male; D008875:Middle Aged; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D012016:Reference Values; D012044:Regression Analysis; D010959:Tissue Plasminogen Activator / Q000097:blood; D014280:Triglycerides / Q000097:blood
D000806:Angiotensin-Converting Enzyme Inhibitors; D001552:Benzazepines; D002121:Calcium Channel Blockers; D007328:Insulin; D017395:Plasminogen Activator Inhibitor 1; D014280:Triglycerides; D017311:Amlodipine; D002784:Cholesterol; D010959:Tissue Plasminogen Activator; C044946:benazepril